Suppression of cellular immunity by lyme disease spirochete Borrelia burgdorferi

Abstract

Modulation of in vitro cellular immune responses by the spirochete Borrelia burgdorferi, the bacteria that causes Lyme disease, was demonstrated. When cultured in the presence of sonicated Borrelia preparation (Bb), the mitogen- or antigen-stimulated proliferative responses of normal lymphocytes were consistently lowered as compared with control values. The degree of the proliferation reduction was directly proportional to both Bb quantity and length of exposure in culture. Bb caused the greatest reduction in both Con A and specific antigen such as BCG-stimulated proliferation, where an almost 100% reduction in proliferation could be achieved. Bb also reduced PHA- or PWM-stimulated PBL proliferation, with the PWM proliferation being the least affected. Also, IL2 production was significantly reduced from Bb-exposed lymphocytes. The entry of Bb-exposed lymphocytes into the proliferating phases of the cell cycle was also shown to be blocked. This regulatory activity was determined to be Bb proteins, sensitive to trypsin treatment and estimated to be 62–100 kDa in molecular weight. Therefore, the presence of spirochetes or their antigens in the hosts may block lymphocyte proliferation and activation, underscoring an important pathogenic mechanism of Lyme disease.